DAT-delivered astaxanthin reprograms adipogenesis through RhoGDI1 dephosphorylation at Ser174 and RhoA/FAK/ERK1/2 cascade suppression.
Hou Y., Zhang Y., Ma Z., Chen X., Xiao Y., Zhong Y.
Animal Study, published in Biomaterials (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Biomaterials (2026)
- Country
- Netherlands
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 41506140
- DOI
- 10.1016/j.biomaterials.2026.123979
Abstract (original English)
Adipose tissue serves as a primary approach for soft tissue defect repair, but clinical regeneration remains limited by inadequate adipogenic capacity. While astaxanthin (AST) can ameliorate adipose dysfunction, the underlying mechanisms governing its pro-adipogenic activity remain elusive. Here, we developed an AST-loaded decellularized adipose tissue (DAT) hydrogel with the aim of boosting adipogenic potential. Subcutaneous implantation of DAT-AST hydrogel into rabbit inguinal fat pad defects significantly enhanced adipogenesis and tissue restoration. In human adipose-derived stem cells (ADSCs), astaxanthin significantly promoted the adipogenic differentiation by suppressing phosphorylation of RhoGDI1 at Ser174 - a newly identified AST-binding target. RhoGDI1 knockdown abolished AST-induced lipid accumulation and disrupted RhoGDI1 related signaling axis (RhoA/FAK/ERK1/2), demonstrating that RhoGDI1 dephosphorylation is essential for AST's pro-adipogenic action. Collectively, this work reveals a targetable pathway for adipose regeneration and establishes DAT as a promising delivery platform for AST therapeutics.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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